Imatinib mesylate elicits extracellular signal-related kinase (ERK) activation and enhances the survival of γ-irradiated epithelial cells

Lee, Jeeyong; Ko, Jiwon; Kim, Hyunji; Im, Hyuntaik; Kim, Sang Hyun; Yi, Jianxun

doi:10.1016/j.bbrc.2018.10.095

Cited by 3 publications

(3 citation statements)

References 15 publications

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“…Moreover, drug monotherapies are not recommended for the treatment of fibrosarcoma. Tyrosine kinases are also important therapeutic targets because of their role in regulating growth factor signaling (Cardoso, Vaz1, Carvalho, Figueira, & Socorr, 2019;Lee et al, 2018). Tyrosine kinases are also important therapeutic targets because of their role in regulating growth factor signaling (Cardoso, Vaz1, Carvalho, Figueira, & Socorr, 2019;Lee et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…Current multidrug therapies include topoisomerase II inhibitors such as doxorubicin and etoposide together with DNA alkylating agents such as ifosfamide (Maswadeh, Aljarbou, Alorainy, Alsharidah, & Khan, 2015). Imatinib mesylate (IMA) is a smallmolecule tyrosine kinase inhibitor that disrupts signaling via receptors implicated in cell proliferation and differentiation such as platelet-derived growth factor receptor (PDGFR), c-Kit, fibroblast growth factor receptor (FGFR)-1, and vascular endothelial growth factor receptor (Cardoso et al, 2019;Lee et al, 2018. Imatinib mesylate (IMA) is a smallmolecule tyrosine kinase inhibitor that disrupts signaling via receptors implicated in cell proliferation and differentiation such as platelet-derived growth factor receptor (PDGFR), c-Kit, fibroblast growth factor receptor (FGFR)-1, and vascular endothelial growth factor receptor (Cardoso et al, 2019;Lee et al, 2018.…”

Section: Introductionmentioning

confidence: 99%

“…Tyrosine kinases are also important therapeutic targets because of their role in regulating growth factor signaling (Cardoso, Vaz1, Carvalho, Figueira, & Socorr, 2019;Lee et al, 2018). Imatinib mesylate (IMA) is a smallmolecule tyrosine kinase inhibitor that disrupts signaling via receptors implicated in cell proliferation and differentiation such as platelet-derived growth factor receptor (PDGFR), c-Kit, fibroblast growth factor receptor (FGFR)-1, and vascular endothelial growth factor receptor (Cardoso et al, 2019;Lee et al, 2018. IMA is used clinically for various cancer types such as gastrointestinal stromal tumors, dermatofibrosarcoma protuberans, aggressive fibromatosis, malignant melanoma, and chordoma (Iqbal & Iqbal, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Efficacy of targeted liposomes and nanocochleates containing imatinib plus dexketoprofen against fibrosarcoma

Çoban

Değim

Yılmaz³

et al. 2019

Drug Development Research

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The main challenges in treating cancer using chemotherapeutics are insufficient dose at the target site and the development of drug resistance, while higher doses can induce side effects by damaging nontarget tissues. Combinatorial drug therapy may overcome these limitations by permitting lower doses and more specific targeting, thereby mitigating drug resistance and nontarget side effects. Recent reports indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) have anticancer potential and can be used together with conventional chemotherapeutics to improve efficacy and safety. In the present study, imatinib mesylate and dexketoprofen trometamol were selected as model drugs to develop targeted surface-modified liposome and nanocochleate formulations for fibrosarcoma treatment. The physicochemical properties and in vitro efficacy of various formulations were evaluated by measurement of particle size distribution, polydispersity index, zeta potential, encapsulation efficiency, diffusion through Caco-2 cells, and toxicity in culture. Selected formulations were then evaluated in fibrosarcoma-bearing model mice by histopathological observations and tyrosine kinase receptor inhibition assays.The most effective formulation on the fibrosarcoma model was a PEGylated nanocochleate formulation. These findings provide a foundation for developing more effective formulations and chemotherapeutic strategies for the treatment of fibrosarcoma and other types of cancer.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Efficacy of targeted liposomes and nanocochleates containing imatinib plus dexketoprofen against fibrosarcoma

Çoban

Değim

Yılmaz³

et al. 2019

Drug Development Research

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AKR1C3 decreased CML sensitivity to Imatinib in bone marrow microenvironment via dysregulation of miR-379-5p

Pan

Yang

Zeng

et al. 2021

Cellular Signalling

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Fibrosis: Types, Effects, Markers, Mechanisms for Disease Progression, and Its Relation with Oxidative Stress, Immunity, and Inflammation

Antar

Ashour

Marawan

et al. 2023

IJMS

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Most chronic inflammatory illnesses include fibrosis as a pathogenic characteristic. Extracellular matrix (ECM) components build up in excess to cause fibrosis or scarring. The fibrotic process finally results in organ malfunction and death if it is severely progressive. Fibrosis affects nearly all tissues of the body. The fibrosis process is associated with chronic inflammation, metabolic homeostasis, and transforming growth factor-β1 (TGF-β1) signaling, where the balance between the oxidant and antioxidant systems appears to be a key modulator in managing these processes. Virtually every organ system, including the lungs, heart, kidney, and liver, can be affected by fibrosis, which is characterized as an excessive accumulation of connective tissue components. Organ malfunction is frequently caused by fibrotic tissue remodeling, which is also frequently linked to high morbidity and mortality. Up to 45% of all fatalities in the industrialized world are caused by fibrosis, which can damage any organ. Long believed to be persistently progressing and irreversible, fibrosis has now been revealed to be a very dynamic process by preclinical models and clinical studies in a variety of organ systems. The pathways from tissue damage to inflammation, fibrosis, and/or malfunction are the main topics of this review. Furthermore, the fibrosis of different organs with their effects was discussed. Finally, we highlight many of the principal mechanisms of fibrosis. These pathways could be considered as promising targets for the development of potential therapies for a variety of important human diseases.

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Imatinib mesylate elicits extracellular signal-related kinase (ERK) activation and enhances the survival of γ-irradiated epithelial cells

Cited by 3 publications

References 15 publications

Efficacy of targeted liposomes and nanocochleates containing imatinib plus dexketoprofen against fibrosarcoma

Efficacy of targeted liposomes and nanocochleates containing imatinib plus dexketoprofen against fibrosarcoma

AKR1C3 decreased CML sensitivity to Imatinib in bone marrow microenvironment via dysregulation of miR-379-5p

Fibrosis: Types, Effects, Markers, Mechanisms for Disease Progression, and Its Relation with Oxidative Stress, Immunity, and Inflammation

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